Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer

ABSTRACT: HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer

PROVIDER: PRJNA732187 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14627784_1.fastq.gz	Fastqsanger.gz
	SRR14627784_2.fastq.gz	Fastqsanger.gz
	SRR14627785_1.fastq.gz	Fastqsanger.gz
	SRR14627785_2.fastq.gz	Fastqsanger.gz
	SRR14627786_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

HDAC5 modulates PD-L1 expression and cancer immunity via p65 deacetylation in pancreatic cancer

Project description:We performed HDAC5 knockdown in pancreatic cancer cell line (PANC-1). The expression profiling showed NF-κB signaling as a potential HDAC5 targets and the conclusions were futher validated in vivo and in vitro.

2022-03-15 | GSE175374 | GEO

HDAC5 loss impairs RB repression of oncogenic related genes and confers CDK4/6 inhibitor resistance in cancer [ChIP-seq]

Project description:The tumor suppressor protein RB acts as a transcription repressor via the interaction of its pocket domain with an L/IXCXE motif in HDAC proteins such as HDAC1. Here we demonstrated that while lacking an L/IXCXE motif, HDAC5 interacts with both RB-N (via an FXXXV motif) and RB-C segments and this interaction is diminished by RB serine-249/threonine-252 and threonine-821 phosphorylation. HDAC5 gene is frequently downregulated or deleted in human cancers such as prostate cancer. Loss of HDAC5 increases histone H3 lysine 27 acetylation (H3K27-ac) and circumvents RB-mediated repression of cell cycle-related oncogenic genes. Accordingly, HDAC5 loss confers resistance to the CDK4/6 inhibitors such as Palbociclib in prostate cancer cells in vitro and in mice, but this effect is overcome by the BET-CBP/p300 dual inhibitor NEO2734. Our findings reveal an unknown role of HDAC5 in RB-mediated histone deacetylation and gene repression and a mechanism modulating CDK4/6 inhibitor therapeutic sensitivity in cancer cells.

2021-07-24 | GSE155003 | GEO

HDAC5 loss impairs RB repression of oncogenic related genes and confers CDK4/6 inhibitor resistance in cancer [RNA-seq]

2021-07-24 | GSE155001 | GEO

TET2 inhibits PD-L1 gene expression in breast cancer cells through histone deacetylation

Project description:TET2 inhibits PD-L1 gene expression in breast cancer cells through histone deacetylation

| PRJNA688657 | ENA

HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3 to suppess gene expression. To identify the target genes of HDAC5, we performed ChIP-seq analysis in FLAG-tagged HDAC5 PDAC escaper cells. HDAC5 binding chromatins were pulled down by HDAC5 antibody and FLAG antibody as replicates.

2020-04-27 | GSE129549 | GEO

RB tumor suppressor promotes cancer immunity through downregulating PD-L1 expression

Project description:Aberrant expression of immune checkpoint protein programmed death ligand-1 (PD-L1) promotes immune tolerance in cancer. RB is a tumor suppressor known to regulate the cell cycle, DNA damage response, and differentiation. Here, we demonstrate transient knockdown or homozygous deletion of RB markedly induces PD-L1 mRNA expression. RB binds to NFκB protein p65 and serine-249/threonine-252 (S249/T252) phosphorylation of RB is important for its interaction with p65 and suppression of PD-L1 expression. RNA-seq analysis identifies a subset of NFκB pathway genes including PD-L1 are selectively upregulated by RB knockdown. S249/T252-phosphorylated RB inversely correlates with PD-L1 expression in patient samples. Expression of a RB-derived S249/T252 phospho-mimicking peptide blocks radiation-induced PD-L1 expression and increases the anti-cancer efficacy of radiation in mice. Our findings reveal a previously unappreciated tumor suppressor function of hyperphosphorylated RB in inhibition of NFκB activity and PD-L1 expression, suggesting this regulatory module can be exploited to overcome cancer immune evasion.

2018-11-19 | GSE109724 | GEO

HDAC5 regulates arachidonic acid metabolism via cPLA2

Project description:We performed HDAC5 knockdown in pancreatic cancer cells along with RNA sequencing. The result helped us to verify that HDAC5 regulates GATA1 dependent cPLA2 expression and arachidonic acid metabolism.

2022-10-11 | GSE185837 | GEO

HDAC5 loss in pancreatic cancer induces enhanced arachidonic acid metabolism via overactivated GATA1-cPLA2 axis

Project description:Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. Additionally, HDAC5’s expression correlates negatively with arachidonic acid (AA) metabolism, which is highly implicated in inflammatory responses and cancer progression. This study aimed to elucidate the role of HDAC5 in AA metabolism and its prospect in the treatment of pancreatic cancer.

2023-08-01 | GSE207863 | GEO

RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in escaper cells, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells knocking down of HDAC5 or scramble shRNA control.

2020-04-27 | GSE149127 | GEO

p65

Project description:p65

| PRJNA811604 | ENA